Clinical significance and prevalence of subarachnoid hyperdensities on flat detector CT after mechanical thrombectomy: does it really matter?

BACKGROUND: Subarachnoid hyperdensities after mechanical thrombectomy (MT) are a common finding. However, it is often regarded as clinically insignificant. OBJECTIVE: With this single-center investigation, to identify the prevalence of subarachnoid hyperdensities following MT, associated predictors, and the impact on the clinical outcome of the patients. METHODS: 383 patients from the stroke registry were analyzed for the presence of subarachnoid hyperdensities on flat detector CT (FDCT) directly after the completion of MT, and on follow-up dual-energy CT, then classified according to a visual grading scale. 178 patients were included with anterior circulation occlusions. Regression analysis was performed to identify significant predictors, and Kruskal-Wallis analysis and Χ2 test were performed to test the variables among the different groups. The primary outcome was the modified Rankin Scale (mRS) score at 90 days and was analyzed with the Wilcoxon-Mann-Whitney rank-sum test. RESULTS: The prevalence of subarachnoid hyperdensities on FDCT was (66/178, 37.1%) with patients experiencing a significant unfavorable outcome (P=0.035). Significantly fewer patients with subarachnoid hyperdensities achieved a mRS score of ≤3 at 90 days 25/66 (37.9%) vs 60/112 (53.6%), P=0.043). In addition, mortality was significantly higher in the subarachnoid hyperdensities group (34.8% vs 19.6%, P=0.024). Distal occlusions and a higher number of device passes were significantly associated with subarachnoid hyperdensities (P=0.026) and (P=0.001), respectively. Patients who received intravenous tissue plasminogen activator had significantly fewer subarachnoid hyperdensities (P=0.029). CONCLUSIONS: Postinterventional subarachnoid hyperdensities are a frequent finding after MT and are associated with neurological decline and worse functional outcome. They are more common with distal occlusions and multiple device passes.

Late-Onset Vaccine-Induced Immune Thombotic Thrombocytopenia (VITT) with Cerebral Venous Sinus Thrombosis.

OBJECTIVES: Vaccine-induced thrombotic thrombocytopenia (VITT) is a rare complication after adenoviral vector vaccination against COVID-19 reported up to 24 days after ChAdOx1 nCOV-19 (AZD1222) vaccination. This report describes a case with a significantly later onset of VITT with cerebral venous sinus thrombosis. CASE DESCRIPTION: We report a 42-year-old woman presenting to the emergency department 53 days after AZD1222 vaccination with sudden onset sensory aphasia and an 18-day history of headache. Cranial computed tomography (CT) showed acute intracranial hemorrhage and CT venogram demonstrated thrombosis of the left vein of Labbé and transverse and sigmoid sinus. D-dimers were elevated and despite a normal platelet count, platelet-activating anti-PF4 antibody testing was positive, confirming the diagnosis of VITT. The patient was treated with intravenous immunoglobulins and argatroban, and was discharged without any neurological deficit on day 12. CONCLUSION: Our report of VITT with symptom onset on day 35 and diagnosis of cerebral sinuous thrombosis on day 53 after AZD1222 vaccination significantly enhances the time window during which VITT may occur.

Diagnostic Accuracy of Quantitative Imaging Biomarkers in the Differentiation of Benign and Malignant Vertebral Lesions : Combination of Diffusion-Weighted and Proton Density Fat Fraction Spine MRI.

PURPOSE: To compare and combine the diagnostic performance of the apparent diffusion coefficient (ADC) derived from diffusion-weighted imaging (DWI) and proton density fat fraction (PDFF) derived from chemical-shift encoding (CSE)-based water-fat magnetic resonance imaging (MRI) for distinguishing benign and malignant vertebral bone marrow lesions (VBML). METHODS: A total of 55 consecutive patients with 53 benign (traumatic, inflammatory and primary) and 36 malignant (metastatic and hematologic) previously untreated VBMLs were prospectively enrolled in this IRB-approved study and underwent sagittal DWI (single-shot spin-echo echo-planar with multi-slice short TI inversion recovery fat suppression) and CSE-based MRI (gradient-echo 6­point modified Dixon) in addition to routine clinical spine MRI at 1.5 T or 3.0 T. Diagnostic reference standard was established according to histopathology or imaging follow-up. The ADC = ADC (0, 800) and PDFF = fat / (water + fat) were calculated voxel-wise and examined for differences between benign and malignant lesions. RESULTS: The ADC and PDFF values of malignant lesions were significantly lower compared to benign lesions (mean ADC 861â€¯× 10-6 mm2/s vs. 1323â€¯× 10-6 mm2/s, p < 0.001; mean PDFF 3.1% vs. 28.2%, p < 0.001). The areas under the curve (AUC) and diagnostic accuracies were 0.847 (p < 0.001) and 85.4% (cut-off at 1084.4â€¯× 10-6 mm2/s) for ADC and 0.940 (p < 0.001) and 89.9% for PDFF (cut-off at 7.8%), respectively. The combined use of ADC and PDFF improved the diagnostic accuracy to 96.6% (malignancy if ADC ≤ 1118.2â€¯× 10-6 mm2/s and PDFF ≤ 20.0%, otherwise benign). CONCLUSION: Quantitative evaluation of both ADC and PDFF was useful in differentiating benign VBMLs from malignancy. The combination of ADC and PDFF improved the diagnostic performance and yielded high diagnostic accuracy for the differentiation of benign and malignant VBMLs.

Fibroblast growth factor receptor 1 gene amplification in gastric adenocarcinoma.

Gastric adenocarcinomas are associated with a poor prognosis due to the fact that the tumor has often metastasized by the time of diagnosis. Thus, identification of novel therapeutic targets is highly desirable. Here, we examined gene copy number of fibroblast growth factor receptor 1 (FGFR1), a potential target for tyrosine kinase inhibitors, and clinicopathologic parameters in a large cohort of gastric adenocarcinomas. We performed fluorescence in situ hybridization analysis of 293 gastric adenocarcinomas using tissue microarrays. Amplification of the FGFR1 gene is a rare but noticeable event that can be found in 2% (6/293) of cases and was associated with poor 10-year survival (median 15.3 months in FGFR1-amplified cases versus 36 months in nonamplified cases, P = .047) and a higher rate of distant metastasis (P = .025). FGFR1 appears to represent a potential new therapeutic target in a subset of patients with gastric carcinoma. Identification of gastric cancers harboring FGFR1 amplification may be important in preselecting patients and/or interpreting clinical studies using tyrosine kinase inhibitors.

Fibroblast growth factor receptor 1 gene amplification in pancreatic ductal adenocarcinoma.

AIMS: Pancreatic ductal adenocarcinomas (PDACs) are chemoresistant, resulting in extremely poor survival of patients; therefore, novel molecular targets, even in small subsets of genetically characterized tumours, are urgently needed. Tyrosine kinase receptor inhibitors (TKIs) are already in clinical use. The aims of this study were to examine the gene copy number and expression of fibroblast growth factor receptor 1 (FGFR1) in 155 patients with PDAC, and investigate the effects of the FGFR-specific inhibitor BGJ398 on FGFR1-amplified pancreatic tumour cells in vitro. METHODS AND RESULTS: Fluorescence in-situ hybridization (FISH) and immunohistochemical analysis of 155 PDACs were performed using tissue microarrays. Amplification of FGFR1 was found in 2.6% (4/155) of cases. Four per cent of tumours (5/125) were shown to express FGFR1 by immunohistochemistry. Sequence analysis demonstrated an activating KRAS mutation (exon 2) in all FGFR1-amplified cases. The FGFR1-amplified pancreatic carcinoma cell line PT45P1 showed high levels of FGFR1 mRNA and protein expression. Proliferation of this cell line can be inhibited using the FGFR1 inhibitor BGJ398. CONCLUSIONS: FGFR1 represents a potential new therapeutic target in a subset of patients harbouring FGFR1-amplified tumours. Identification of pancreatic cancers harbouring FGFR1 amplification may be important in preselecting patients and/or interpreting clinical studies using TKIs.